[Ulcerative colitis and proctitis in two Swiss Braunvieh cows]. / Ulzerierende Colitis und Proktitis bei zwei Braunviehkühen.

Two Swiss Braunvieh cows were referred to our clinic because of narrowing of the rectum and difficult rectal examination attributable to restricted arm movement within the pelvic cavity. Cow 1 also had perforation of the cranial rectum and cow 2 had multiple small funnel-shaped depressions in the rectal mucosa. Both cows had ultrasonographic evidence of peritonitis with thickening of the intestinal wall and fibrin and fluid accumulation in the abdominal cavity. A diagnosis of peritonitis was made in both cows, most likely caused by rectal perforation; they were euthanized and a post-mortem examination was carried out. Both cows had proctitis and ulcerative colitis with three or four perforated ulcers which were associated with fibrinopurulent peritonitis. The final diagnosis was ulcerative colitis and proctitis of unknown aetiology. Infectious causes of colitis and proctitis, including bovine viral diarrhoea, adenovirus infection and salmonellosis, and trauma and poisoning were ruled out.

Focal eosinophilic proctitis with associated rectal prolapse in a pony.

Focal intramural nodules were palpated in the rectal wall of a 12-year-old pony mare presented for rectal prolapse. Eosinophilic proctitis was diagnosed by examination of fine needle aspirates and biopsy of the largest rectal nodule. After treatment with a course of corticosteroids, the rectal nodule and accompanying peripheral eosinophilia resolved. There was no recurrence of the condition during the follow-up period of 20 months. Focal eosinophilic proctitis appeared to be an unusual cause of tenesmus and rectal prolapse in this case.

Rectal stricture in an ostrich (Struthio camelus).

Exploratory celiotomy of an 18-mo-old female ostrich (Struthio camelus) with anorexia, lethargy, and constipation of 5 days' duration showed mesenteric volvulus and a focal narrowing of the rectum approximately 28 cm cranial to the cloaca. The prognosis was poor and the animal was euthanized. Necropsy revealed a fibrinonecrotic proctitis and a 3-cm-long circumferential stricture of the rectum. Histologically, the rectal wall at the stricture was deeply effaced by fibrovascular connective tissue with vascular thrombosis and necrotizing vasculitis, and it resembled the lesions in feeder pigs with fibrinonecrotic colitis.

Inflammatory large bowel disease in immunodeficient rats naturally and experimentally infected with Helicobacter bilis.

Proliferative and ulcerative typhlitis, colitis, and proctitis were found incidentally in a breeding colony of male athymic nude (Cr:NIH-rnu) rats. Within the crypts of the large intestine, modified Steiner's silver stain revealed spiral organisms that were identified by culture, polymerase chain reaction, and sequencing to be Helicobacter bilis. The large bowel disease was reproduced in H. bilis-free male athymic nude rats that were injected intraperitoneally with a culture of H. bilis from the affected colony. The organism was isolated from the feces and cecum of the experimentally infected rats. H. bilis should be considered a potential pathogen in immunocompromised rats. The infection in immunocompromised rats may serve as an animal model for inflammatory large bowel disease.

Intracellular Campylobacter-like organisms associated with rectal prolapse and proliferative enteroproctitis in emus (Dromaius novaehollandiae).

Rectal prolapse was the presenting clinical finding in a group of juvenile emus (Dromaius novaehollandiae). Gross findings included severely thickened and rugose distal rectal mucosae. Histologically, there were thickened villi, enterocyte hyperplasia, dilated glands filled with mucus and heterophils, and a dense infiltrate of heterophils, macrophages, lymphocytes, and plasma cells in the lamina propria. Examination of Warthin-Starry silver-stained sections revealed numerous apically located comma-shaped intracytoplasmic bacteria approximately 1 x 3 microns in size. Campylobacter-like organisms morphologically compatible with ileal symbiont intracellularis now known as Lawsonia intracellularis were seen via electron microscopy. Bacteria were further characterized by indirect immunofluorescence using monoclonal antibody specific for the 25-27-kd outer membrane protein of L. intracellularis.

Proctitis associated with chlamydial infection in a koala.

OBJECTIVE: To describe proctitis associated with chlamydial infection in a koala. DESIGN: A pathological study. ANIMAL: A free living, male koala aged 17 years. PROCEDURE: Rectum was examined histologically and chlamydial organisms visualised using Giminez' stain and an immunoperoxidase staining method using an anti-Chlamydia lipopolysaccharide (genus specific) antibody. RESULTS: An aged koala presented for euthanasia was found to have asymptomatic chronic proctitis, cystitis, prostatitis, urethritis and conjunctivitis associated with chlamydial infection. Inflammation was severe in the terminal rectum and extended into the proximal common vestibule. Chlamydial organisms were visualised in the rectal surface epithelium using Giminez' stain and an immunoperoxidase staining method. Organisms were also detected in the epithelium of the bladder, prostate and urethra. CLINICAL IMPLICATIONS: Possible modes of transmission for the rectal infection are direct sexual transmission or ascending infection by organisms shed from the urogenital tract into the common vestibule. Previously unreported chlamydial proctitis in the koala may represent a potential reservoir of infection for other koalas.

Rectal biopsy diagnosis in horses with clinical signs of intestinal disorders: a retrospective study of 116 cases.

The histology from rectal biopsy specimens taken 1980-1990 on 131 occasions from 116 horses, age 1-18 years, with clinical signs of intestinal disease was evaluated and classified retrospectively. In 40 horses, autopsy results were studied for comparison. Biopsy specimens (21 horses) and post mortem rectal tissue (9 horses) from 30 healthy horses, age 4-22 years, were used as controls. In 105 clinical cases, a biopsy was performed on only one occasion, while repeat biopsy was performed in 11 cases. Specimens showed pathological changes in 60 horses. The findings were classified into acute, chronic or chronic active simple proctitis, granulomatous enteritis, eosinophilic granulomatosis/gastroenteritis, eosinophilic proctitis, erosive/ulcerative proctitis, pseudomembranous proctitis, proctitis with vasculitis and malignant lymphoma. Mild scattered neutrophil infiltration in the lamina propria was found in controls, but neutrophils in crypt or surface epithelia were abnormal findings. Depletion or hyperplasia of goblet cells sometimes accompanied inflammation. Simple proctitis occurred in association with malignant lymphoma and various inflammatory disorders of the gastrointestinal tract apparent at autopsy. Eosinophilic granulomatosis/gastroenteritis and granulomatous enteritis were diagnosed from biopsy specimens in 6 of 12 and 4 of 9 cases, respectively, of these diseases confirmed at autopsy. Reduction of acid mucins in goblet cells was a prominent feature of eosinophilic granulomatosis. Rectal biopsy was found to be a useful adjunct for evaluation of intestinal disease in the horse.

Regional eosinophilic coloproctitis, typhlitis and ileitis in a dog.

A 3-year-old female Petit Basset Griffon Vendeen is presented with tenesmus alvi caused by a 15 cm long chronic regional cicatrising eosinophilic coloproctitis with bacterial masses surrounded by clubs, resembling actinomycosis. Similar changes were found in the caecum, next to a nodular eosinophilic inflammation in the ileal mucosa.

Follow-up studies by large intestinal biopsies and necropsy in dogs with clinical signs of large bowel disease.

The results of follow-up studies in 77 dogs with clinical signs of large bowel disease are presented. In 32 dogs colonic and/or rectal biopsy follow-up studies were done, combined with necropsy in seven dogs. In 45 dogs a follow-up necropsy only was done. The time between the first and the last series of biopsies varied from three to 729 days and between the first series of biopsies and necropsy from one to 980 days. Colitis found in 45 dogs in the initial biopsies was still present in 29 cases in the follow-up biopsy studies and/or at necropsy. Eleven cases showed hystiocytic ulcerative colitis. In general, adenoma, carcinoma and lymphosarcoma were confirmed in the follow-up examination, except for one adenoma, which appeared to be a carcinoma at necropsy. In cases in which the differential diagnosis was adenoma or carcinoma, the necropsy diagnosis was always carcinoma and in cases of a differential diagnosis of lymphosarcoma and/or colitis, lymphosarcoma was always diagnosed at necropsy. Several dogs without colonic changes in the initial biopsies had other gastric or small intestinal lesions at necropsy such as gastritis and enteritis of the small intestine, or tumors, in these areas.

A retrospective evaluation of the rectal pull-through technique. Procedure and postoperative complications.

Ten animals (8 dogs and 2 cats) with distal rectal lesions were treated by surgically resecting the affected segment of the rectum by the rectal pull-through technique. There were four malignant tumors, three benign tumors, two inflammatory lesions, and one malignant tumor that extended histologically to the margins of a previous surgical excision. Postoperative complications were tenesmus (7 animals), fecal incontinence (4 animals), rectal bleeding (4 animals), and abscess formation (1 animal). Dehiscence and stricture were not observed. The four animals with malignant tumors survived less than 12 months after surgery. One of the four animals still living has persistent fecal incontinence. The rectal pull-through technique is described and illustrated.

The pathogenesis of porcine rectal stricture. I. The naturally occurring disease and its association with salmonellosis.

Rectal stricture occurred in each of 23 pigs submitted for necropsy from eight Indiana farms. Each stricture was an annular cicatrization of the rectal wall, 2.0-5.0 cm anterior to the anorectal junction. Emaciation, colonic dilatation and compression atrophy of abdominal and thoracic viscera were a result of chronic obstipation and inanition. Most pigs with strictures had severe enteric disease 4-8 weeks before the strictures occurred. Salmonella typhimurium was isolated from seven of the eight groups of pigs examined. Ulcerative proctitis, a possible precursor of rectal stricture, was frequently in pigs with enterocolitis caused by S. typhimurium.

The pathogenesis rectal stricture. II. Experimental salmonellosis and ischemic proctitis.

Experimentally induced oral Salmonella typhimurium infection in pigs resulted in a severe, prolonged enterocolitis with ulcerative proctitis a constant feature. Healed lesions were annular cicatricial ulcers in the part of the rectum affected with rectal strictures. Strictures indistinguishable from the naturally occurring lesion were produced by injecting chlorpromazine into the cranial hemorrhoidal artery of three pigs. Dye injected into the cranial hemorrhoidal artery perfused the entire rectum in normal pigs, but in pigs with either rectal stricture or salmonella proctitis the dye halted at the cranial margin of the transverse mucosal defect. The predilection of rectal stricture and its proposed precursor, salmonella ulcerative proctitis, for the middle third of the rectum was attributed to a normally precarious arterial supply which renders the rectum unusually susceptible to ischemic injury and decreases its reparative capacity.